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PubMed2003

Cochlear blood flow modifications induced by anaesthetic drugs in middle ear surgery: comparison between sevoflurane and propofol.

OBJECTIVE: Because it is necessary to maintain controlled hypotension during middle ear surgery in order to avoid bleeding and as it is known that cochlear blood flow (CBF) is related to blood pressure (BP), it is useful to evaluate CBF modifications induced by anaesthetics in order to prevent cochlear damage. The aim of this paper is to evaluate, using laser Doppler flowmetry, which anaesthetic drug, out of sevoflurane and propofol, has the smallest effect on CBF. MATERIAL AND METHODS: Twenty consenting adult patients scheduled for myringoplasty under general anaesthesia for simple tympanic membrane perforation were studied. Patients were divided into two groups: the first group was treated with sevoflurane and the second with propofol. For the first group, CBF measurement was carried out on three different occasions: (i) at a basal low drug dosage; (ii) having increased the drug dosage to a higher level; and (iii) having reduced the drug dosage to the basal low level again. For the second group, CBF measurement was carried out on three different occasions: (i) 10 min after injecting a bolus of propofol; (ii) immediately after a second propofol injection; and (iii) 10 min after a third injection of propofol. A probe was placed over the promontory in order to measure CBF levels. RESULTS: In the subjects treated with sevoflurane, after having increased the drug dosage, BP decreased significantly while CBF did not change significantly. In the subjects treated with propofol we recorded a significant reduction in BP, as well as a decrease in CBF. CONCLUSION: The results obtained show that sevoflurane has a hypotensive effect without modifying CBF, while propofol, although having a similar effect on BP to sevoflurane, has less of a protective effect on inner ear microcirculation.

Adult↗
PubMed2001

Optical aggregometry versus the PFA-100: experimental studies in pigs treated with propofol.

An experimental study of platelet aggregation was performed in 22 male Landrace x Large-White crossbred pigs treated with propofol at different doses, to compare the results of optical aggregometry with those of the PFA-100 (Dade Int., Miami, FL, USA), a new platelet function analyzer. Platelet aggregation was analyzed in basal blood samples by both methods, after which the pigs were divided into three groups: G1, anaesthetic induction with propofol (2 mg/kg intravenously (i.v.)); G2, anaesthetic induction with propofol (2 mg/kg i.v.), followed by a second dose of 1.5 mg/kg; and G3, anaesthetic induction with propofol (2 mg/kg i.v.), followed by 1 h of continuous i.v. infusion at 13 mg/kg/h. Four minutes after propofol injection, blood samples were again taken from each group and studied by both methods. In groups G2 and G3, both methods showed reduced platelet aggregation, while in group G1 neither evidenced an anti-aggregating effect of propofol. Under our experimental conditions: (1) the propofol effect on platelet aggregation depends on the plasma concentration; (2) the results obtained with the two methods are comparable; (3) PFA-100 may provide an alternative to optical aggregometry for detecting the effects of anaesthetic agents ex vivo.

Adenosine Diphosphate↗
PubMed1987

Dose requirements of propofol by infusion during nitrous oxide anaesthesia in man. II: Patients premedicated with lorazepam.

The infusion rate of propofol required to supplement 67% nitrous oxide in oxygen to maintain surgical anaesthesia was determined in 72 patients premedicated with lorazepam. Following an induction dose of propofol 2 mg kg-1, groups of eight patients received an infusion of propofol varying from 60 to 200 micrograms kg-1 min-1. Probit analysis was used to determine the ED50 (130 micrograms kg-1 min-1; 95% confidence limits: 106-167 micrograms kg-1 min-1) and ED95 (348 micrograms kg-1 min-1; 95% confidence limits: 233-1296 micrograms kg-1 min-1) for propofol infusion. Whole blood propofol concentrations at the time of surgical incision correlated strongly with the infusion rate, giving an EC50 value of 2.5 micrograms ml-1, and an EC95 value of 5.92 micrograms ml-1. There was no significant correlation between the rate of infusion of propofol, or the total propofol dose, and the times to response to command, or to recall of birthdate.

Adolescent↗
PubMed1987

Pharmacokinetics of propofol in female patients. Studies using single bolus injections.

The pharmacokinetics of propofol in a dose of 2.5 mg kg-1 given via a vein in the antecubital fossa were studied in 18 patients. Anaesthesia was maintained with nitrous oxide in oxygen in all patients. The effects of pretreatment with fentanyl (n = 6) and maintenance with halothane (n = 6) on the pharmacokinetics of propofol were also investigated. Pretreatment with fentanyl resulted in prolonged apnoea in four patients. No serious side effects occurred. The pharmacokinetics of propofol in unpretreated patients who were maintained with nitrous oxide in oxygen only can be described by a three-compartment open mammalian model with very rapid distribution (T1/2 alpha about 3 min), rapid elimination (T1/2 beta 45 min) and a slower final phase (T1/2 gamma about 300 min). The total body clearance of propofol was rapid (1.91 litre min-1). Propofol was initially distributed into a relatively large central compartment (41.3 litre) and was extensively redistributed (Vss 305 litre; V gamma 722 litre). Throughout the sampling period the mean blood concentrations of propofol for the patients pretreated with fentanyl were about 50% higher than the mean concentrations for patients maintained with nitrous oxide only. Mean propofol concentrations for the patients maintained with halothane were intermediate between those of the other two groups.

Adult↗
PubMed1988

Pharmacokinetics of propofol (diprivan) in elderly patients.

The pharmacokinetics of propofol (2,6 diisopropylphenol) were compared in 12 patients aged 65-80 yr and 12 patients aged 18-35 yr. After premedication with papaveretum i.m., anaesthesia was induced with propofol 2.0 mg kg-1 in the elderly and 2.5 mg kg-1 in the younger patients. Alcuronium 12-20 mg was then given and the patient's lungs ventilated with halothane and nitrous oxide in oxygen. Blood was taken after various time intervals up to 24 h for the measurement of propofol concentrations by HPLC and for the estimation of propofol protein binding. The mean blood propofol concentration was generally higher in the elderly group, but this difference was only significant at 2 min after induction. The clearance of propofol was significantly lower in the elderly (1.44 +/- 0.10 (SE) litre min-1) than in the younger patients (1.79 +/- 0.12 litre min-1). The volume of the central compartment in the elderly patients was significantly smaller (19.6 +/- 5.2 litre) than that in the young (26.3 +/- 2.9 litre). There was no difference in the volume of distribution at equilibrium (1608 +/- 246 litre in the elderly and 1757 +/- 360 litre in the young), in the volume of distribution at steady state (691 +/- 139 litre in the elderly and 771 +/- 236 litre in the young) or in the half-lives of distribution and elimination. The plasma protein binding of propofol was similar in both groups and showed no trend with time after dose.

Adult↗
PubMed1992

Extrahepatic metabolism of propofol in man during the anhepatic phase of orthotopic liver transplantation.

We have investigated extrahepatic metabolism of propofol in 10 patients undergoing orthotopic liver transplantation (group 1) (mean age 38 yr, mean weight 60 (SD 7) kg) and compared it with that in 10 patients without liver dysfunction undergoing extrahepatic abdominal surgery (group 2) (mean age 56 yr, mean weight 68 (11) kg). A single i.v. bolus dose of propofol 0.5 mg kg-1 was injected into a peripheral vein 5 min after the beginning of the anhepatic phase in group 1 and 60 min after the induction of anaesthesia in group 2. Arterial blood samples were obtained at 5, 10, 15, 20, 30, 40, 50 and 60 min after injection and urine samples were collected every 15 min. Propofol concentrations in whole blood and urine were measured by high performance liquid chromatography with fluorescence detection. Propofol glucuronide was measured in urine by incubation with a specific beta-glucuronidase. The area under the time-blood concentration curve from 0 to 60 min was found to be significantly greater in group 1 (13743 (2830) micrograms litre-1 h-1) than in group 2 (7992 (4895) micrograms litre-1 h-1) (P less than 0.05). Unchanged propofol was not detected in the urine of either group. No significant difference was found in the amount of propofol glucuronide excreted by patients in group 1 (457 (269) micrograms) and in group 2 (921 (672) micrograms). The presence of a propofol metabolite in urine when the liver was excluded from the circulation suggests that extrahepatic metabolism occurred.

Adult↗
PubMed1992

Synergistic interaction between midazolam and propofol.

We gave either midazolam or propofol for induction of anaesthesia to 140 ASA I or II female patients (18-60 yr). ED50 values were obtained by probit analysis for three clinical end-points: loss of response to command; loss of eyelash reflex; failure to respond to application of an anaesthetic face mask delivering 1% isoflurane. Propofol ED50 values (95% confidence intervals) were 1.25 (0.99-1.48) mg kg-1, 1.61 (1.29-1.94) mg kg-1 and 1.51 (1.20-1.82) mg kg-1, respectively. ED50 values for midazolam were 0.26 (0.20-0.37) mg kg-1, 0.29 (0.23-0.47) mg kg-1 and 0.25 (0.20-0.32) mg kg-1, respectively. An additional 92 similar patients received one of nine dose combinations of midazolam and propofol for induction of anaesthesia, propofol being administered 2 min after midazolam. Success of induction was based on the clinical end-point of loss of response to command. Administration of 25% of the ED50 of midazolam followed by 50% of the ED50 of propofol resulted in loss of response to command in 50% of patients, while 50% of the ED50 of midazolam, followed by 25% of the ED50 of propofol had the same effect. A probit regression model specifying a synergistic interaction between midazolam and propofol fitted the data significantly better than a model specifying no interaction.

Adolescent↗
PubMed1993

Comparison of CNS effects of propofol and thiopentone in cats.

Using cats with chronically implanted brain electrodes, we have compared the effects of propofol on CNS electrical activities with those of thiopentone. Ten cats were allocated to receive either propofol (n = 5) or thiopentone (n = 5). Cats were anaesthetized initially with 4% halothane in oxygen. The trachea was intubated and the lungs ventilated mechanically. A femoral artery and a vein in a forepaw were cannulated for arterial pressure monitoring and fluid infusion. After the inspired concentration of halothane was maintained at 0.5%, EEG in the cortex, the amygdala and the hippocampus, somatosensory evoked potential (SEP) and reticular multi-unit activity (R-MUA) were recorded. Incremental doses of propofol or thiopentone were administered i.v. at 5-min intervals during 0.5% halothane anaesthesia. The cumulative doses of propofol and thiopentone were 2, 5, 10 and 20 mg kg-1, and 4, 10, 20 and 40 mg kg-1, respectively. Arterial pressure was maintained in excess of 100 mm Hg systolic by infusion of phenylephrine. All cats in the propofol group survived, but two in the thiopentone group died after the administration of thiopentone 40 mg kg-1. Changes observed in CNS activity were dose-related in all cases. The EEG changed with the increments of doses of propofol or thiopentone, from fast, small amplitude to complexes of fast and slow, large amplitude activities, burst suppression and flat EEG. SEP latency was prolonged by both agents: the peak latency of N1 changed from 15 (SD 2) ms to 20 (5) ms with propofol 20 mg kg-1, and from 14 (1) ms to 27 (2) ms with thiopentone 40 mg kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1994

Effects of sub-hypnotic doses of propofol on the side effects of intrathecal morphine.

We have studied the effect of propofol on the side effects associated with intrathecal morphine in 40 patients undergoing major arthroplasty. Patients received spinal anaesthesia with plain 0.5% bupivacaine 20 mg mixed with preservative-free morphine 0.3 mg. Before injection of the local anaesthetic, the patients were allocated randomly to receive either a bolus dose of propofol 10 mg followed by an infusion of 30 mg/24 h or equal volumes of 10% Intralipid (control group). The number of patients without postoperative nausea and vomiting (PONV) was similar in both groups. However, the incidence of nausea and vomiting was lower in the propofol (13 and 22, respectively) than in the control (34 and 36) group (P < 0.01 and P < 0.05, respectively). Severe vomiting episodes were less frequent in the propofol group (1 vs 11; P < 0.05). Four patients in the propofol group and 12 patients in the control group had itching (P < 0.05). The incidence of urinary retention was similar in both groups. There was no additional sedation attributable to propofol. In conclusion, sub-hypnotic doses of propofol protected significantly against itching and had a modest effect on PONV after intrathecal morphine.

Aged↗
PubMed1995

Haemodynamic effects of propofol infusion for sedation after coronary artery surgery.

We have compared the haemodynamic effects of a sedative dose of propofol with placebo (vehicle of propofol) in a randomized, double-blind study in 20 patients immediately after coronary artery bypass grafting (CABG). During a continuous infusion of a mixture of fentanyl and pancuronium, each patient was given in a crossover design, a loading dose of propofol 0.5 mg kg-1 and vehicle over 5 min followed by a continuous infusion of propofol 20 micrograms kg-1 min-1 and vehicle, respectively, for 55 min. Administration of propofol caused a significant decrease in mean arterial pressure (mean change from pre-drug values to those during drug infusion: -15.4% vs +1.3% with placebo; P < 0.001), mean pulmonary artery pressure (-6.5% vs +5.8%; P < 0.001), systemic vascular resistance (-13.8% vs -0.6%; P < 0.05), pulmonary vascular resistance (-2.0% vs +9.0%; P < 0.05), cardiac output (-2.4% vs +2.6%; P < 0.05) and pulmonary artery occlusion pressure (-8.0% vs +1.4%; P < 0.05). Propofol did not affect heart rate, but it tended to decrease stroke volume (P = 0.102). These data suggest that, during the recovery phase from CABG surgery, a short-term infusion of a sedative dose of propofol decreases systemic and pulmonary arterial pressure by decreasing systemic and pulmonary vascular resistance, respectively, and cardiac output. The decrease in cardiac output appeared to be caused mainly by a decrease in stroke volume.

Adult↗
PubMed1997

Propofol anaesthesia and postoperative nausea and vomiting: quantitative systematic review of randomized controlled studies.

We have analysed randomized controlled studies which reported the incidence of postoperative nausea and vomiting (PONV) after propofol anaesthesia compared with other anaesthetics (control). Cumulative data of early (0-6 h) and late (0-48 h) PONV were recorded as occurrence or non-occurrence of nausea or vomiting. Combined odds ratio and number-needed-to-treat were calculated for propofol as an induction or maintenance regimen, early or late outcomes, and different emetic events. This was performed for all control event rates and within a range of 20-60% control event rates. We analysed 84 studies involving 6069 patients. The effect of propofol on PONV was dependent mainly on the method of administration, time of measurement and range of control event rates. When all studies were included the number-needed-to-treat to prevent PONV with propofol was more than 9 when used for induction of anaesthesia and at best 6 when used for maintenance. Within the 20-60% control event rate range, best results were achieved with propofol maintenance to prevent early PONV: the number-needed-to-treat to prevent early nausea was 4.7 (95% confidence interval 3.8-6.3), vomiting 4.9 (4-6.1) and any emetic event 4.9 (3.7-7.1). Within the 20-60% control event rate, of five patients treated with propofol for maintenance of anaesthesia, one will not vomit or be nauseated in the immediate postoperative period who would otherwise have vomited or been nauseated. This may be clinically relevant. In all other situations the difference between propofol and control may have reached statistical significance but was of doubtful clinical relevance. Treatment efficacy should be established within a defined range of control event rates for meaningful estimates of efficacy and for comparisons.

Anesthetics, Intravenous↗
PubMed1997

Effect of propofol on isolated human omental arteries and veins.

To elucidate the effect and mode of action of propofol on human vascular smooth muscle tension, we have investigated the effect of propofol alone and the effect of propofol on contractions induced by U46619, KCl and caffeine on isolated human omental vessels. Propofol 10(-3) mol litre-1 induced contractions in both arteries and veins attenuated the contraction elicited by U46619, KCl and caffeine in a concentration-dependent manner. The threshold concentrations for the effect of propofol in the artery were: 10(-5) mol litre-1 (U46619, caffeine) and 10(-4) mol litre-1 (KCl); and in the vein, 10(-5) mol litre-1 (U46619) and 10(-4) mol litre-1 (KCl, caffeine). We conclude that propofol at lower concentrations appeared to primarily attenuate contraction involving release of cellularly sequestered calcium. At higher concentrations (> 10(-4.5) mol litre-1), propofol appeared to affect contraction involving extracellular or intracellular calcium fluxes similarly.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1997

Effect of lignocaine and pH on propofol-induced pain.

Propofol has the disadvantage of pain on injection. A higher partition of propofol in the aqueous phase of the preparation causes a higher incidence of pain on injection while addition of 1% lignocaine to propofol reduces pain. The low concentration of this local anaesthetic and the rapid pain relief observed indicates that mechanisms other than local anaesthesia are involved, that is change in pH. We performed a clinical study to investigate the influence of lignocaine and pH on pain during injection of 1% Diprivan. Ten parts of 1% Diprivan were mixed with one part of saline, 1% lignocaine or hydrochloric acid to achieve the same pH as that after addition of lignocaine. Diprivan 1% mixed with 1% lignocaine and with hydrochloric acid gave mean pain ratings (1-10) of 0.32 (SD 0.75) (n = 25) and 0.88 (1.30) (n = 24), respectively. These ratings were significantly lower than ratings after injection of a saline-Diprivan mixture (2.18 (2.06), n = 22). The pH of the 1% Diprivan formulation decreased after mixing with 1% lignocaine. The concentration of propofol in the aqueous phase was lower when 1% Diprivan was mixed with 1% lignocaine (0.376 g litre-1) or HCl (0.392 g litre-1) compared with 1% Diprivan and saline (0.476 g litre-1) mixed in the same proportion. Thus pH changes may modify propofol-induced pain on injection by a mechanism different from the effect of the local anaesthetic on the vascular endothelium. Our findings may explain why lignocaine mixed with propofol causes less pain than injection of lignocaine followed by propofol.

Adolescent↗
PubMed1997

Differential effects of nitrous oxide and propofol on myogenic transcranial motor evoked responses during sufentanil anaesthesia.

We have compared the effects of 50% nitrous oxide and propofol, each administered concurrently with sufentanil, on the amplitudes and latencies of the compound muscle action potential (CMAP) response to transcranial electrical stimulation. Using a crossover design, 12 patients undergoing spinal surgery were exposed to both 50% nitrous oxide and propofol, the latter in a bolus-infusion regimen. Six patients received nitrous oxide first and six received propofol first. CMAP were recorded from the tibialis anterior muscle in response to both single and paired transcranial electrical stimuli. With single pulse stimulation, median CMAP amplitude was significantly greater during administration of nitrous oxide than propofol (nitrous oxide 335 (10th-90th percentiles 35-849) microV; propofol 36 (0-251) microV) (P < 0.01). With paired stimulation, there was no significant difference in CMAP amplitude during the two regimens (nitrous oxide 1031 (296-1939) microV; propofol 655 (0-1867) microV). The results indicate that propofol caused more depression of transcranial electrical motor evoked responses than 50% nitrous oxide but that the difference was probably clinically unimportant when a paired stimulation paradigm was used.

Adolescent↗
PubMed1998

Pharmacokinetics of propofol during conscious sedation using target-controlled infusion in anxious patients undergoing dental treatment.

Infusion of propofol by a target-controlled infusion (TCI) system is effective in achieving conscious sedation for anxious patients presenting for dental surgery. It is a common clinical observation that anxious patients require more anaesthetic drugs than non-anxious individuals. In study 1 we have defined blood propofol concentrations necessary for conscious sedation in both anxious (n = 23) and non-anxious (n = 18) patients. The pump performance of the TCI system, using Gepts' pharmacokinetic model, was evaluated in these two patient groups. Subsequently, clearance of propofol was compared in the two groups. Mean measured venous serum propofol concentrations obtained between 20 and 35 min after the optimal sedation level was reached were 1.6 (SD 0.2) micrograms ml-1 in the anxious patients compared with 1.7 (0.3) micrograms ml-1 in the control group (study 1) and 1.4 (0.27) micrograms ml-1 in study 2. The pump systematically overpredicted measured propofol concentrations in both groups (study 1). There was no significant difference in propofol clearance between the two groups. In study 2, an optimized set of microconstants was derived which should more accurately predict the pharmacokinetic profile of the anxious population and this set was tested prospectively in another group of 12 anxious dental patients. Bias and precision with the optimized kinetic set were significantly less than the values obtained in study 1. We conclude that there was no significant pharmacokinetic differences between anxious and non-anxious subjects receiving subanaesthetic doses of propofol for conscious sedation.

Adolescent↗
PubMed1998

Positive pressure ventilation with the laryngeal mask airway in non-paralysed patients: comparison of sevoflurane and propofol maintenance techniques.

We have compared anaesthetic maintenance and emergence characteristics of propofol and sevoflurane with the laryngeal mask airway (LMA) at commonly used doses in 185 ASA I-II patients, in a randomized, prospective study. Anaesthesia was induced with propofol 2.5-3.5 mg kg-1 and fentanyl 1-3 micrograms kg-1. Neuromuscular blocking agents were not used. All patients underwent positive pressure ventilation (PPV) with tidal volumes of 6-8 ml kg-1 to maintain normal end-tidal carbon dioxide concentration. Anaesthesia was maintained with 66% nitrous oxide in oxygen and infusion of propofol 6 or 8 mg kg-1 h-1, or 1% or 1.5% end-tidal sevoflurane. There were no failed insertion attempts and adequate ventilation was achieved in all patients. During emergence, there was a greater incidence of excitatory phenomena with 1% and 1.5% sevoflurane (95% confidence intervals (CI) 4-19%) compared with propofol (95% CI 0-4%). Sevoflurane 1.0% (95% CI 37-71%) was associated with the greatest overall incidence of respiratory and haemodynamic problems. This was significantly higher compared with propofol 6 mg kg-1 h-1 (95% CI 19-36%). Shorter times to LMA removal were observed with 1% and 1.5% sevoflurane compared with propofol (P < 0.0002). Postoperative problems did not differ between groups. We conclude that propofol 6-8 mg kg-1 h-1 and 1.5% sevoflurane were suitable for maintenance of anaesthesia for musculoskeletal surgery in non-paralysed ASA I-II patients undergoing PPV with the LMA. Emergence was more rapid with sevoflurane, but was associated with more excitatory phenomena.

Adult↗
PubMed1998

Effects of premedication on dose requirements for propofol: comparison of clonidine and hydroxyzine.

The influence of a single dose of clonidine (5 micrograms kg-1) or hydroxyzine (1 mg kg-1) on intraoperative propofol requirements was determined in 28 male patients (ASA I) undergoing elective orthopaedic surgery. Patients were randomly allocated to receive either clonidine or hydroxyzine orally 2 h before induction of anaesthesia. After a loading dose of propofol (2.5 mg kg-1), mivacurium (0.2 mg kg-1) and alfentanil (15 micrograms kg-1), anaesthesia was maintained with a standardized propofol infusion supplemented with nitrous oxide (66%) in oxygen. During surgery, additional propofol boluses (1 mg kg-1) were administered when heart rate or mean arterial pressure increased by more than 10% compared with preinduction values. The clonidine group demonstrated a 14.5% decrease in total propofol requirements (P < 0.05) and a 52.2% reduction in additional propofol boluses (P < 0.02) in comparison with the hydroxyzine group. intraoperative heart rate and mean arterial pressure were significantly lower in the clonidine group but no patients needed treatment with ephedrine for hypotension or bradycardia. Recovery of psychomotor function and discharge from the recovery room were not delayed in the clonidine group. This study indicates that 5 micrograms kg-1 clonidine given as premedication in ASA I patients reduces intraoperative propofol requirements in comparison with 1 mg kg-1 hydroxyzine without inducing adverse effects on recovery or haemodynamic stability.

Adolescent↗
PubMed1999

Intracoronary propofol attenuates myocardial but not coronary endothelial dysfunction after brief ischaemia and reperfusion in dogs.

We have investigated the effects of propofol on recovery of regional mechanical and coronary endothelial function and on lipid peroxidation in post-ischaemic myocardium in dogs. The animals were assessed for 180 min during reperfusion after 15-min of occlusion of the left anterior descending coronary artery (LAD). They were treated with intracoronary (i.c.) propofol 5 or 20 micrograms/ml of coronary flow or vehicle (control group) for 60 min, beginning 30 min before LAD occlusion. Propofol significantly enhanced recovery of regional contractile function (70% and 81% of baseline segment shortening in the propofol 5 and 20 micrograms ml-1 groups, respectively, compared with 51% in controls at 3 h of reperfusion). However, LAD flow responses to i.c. acetylcholine were similarly attenuated regardless of treatment with propofol throughout reperfusion. The increase in malondialdehyde induced by ischaemia-reperfusion was significantly suppressed by both doses of propofol. These results demonstrated that in vivo, propofol ameliorated dysfunction of the myocardium but not of the coronary endothelium resulting from brief ischaemia and reperfusion; the protection may be related, at least in part, to its ability to reduce lipid peroxidation.

Anesthetics, Intravenous↗